The conditions conducive to the immunological destruction of syngeneic tumors in mice will be studied. Models of concomitant immunity will be employed to discover why a host that is unable to control the growth of its primary tumor can nevertheless destroy a challenge of cells of the same tumor at another site. This will entail determining the immunological status of the host during tumorigenesis in terms of its capacity to reject a tumor challenge and to produce cytotoxic T cells, B cells, macrophages and other cells. The kinetics of production of these cells will be correlated with change in the host's capacity to focus them at the site of a tumor cell challenge. A comparison between the cytological and humoral events that occur at the site of a threshold and an above-threshold (escape dose) challenge of tumor cells will provide information about blocking factors or other factors that supress the action of effector cells at the tumor site. A model which employs Corynebacterium parvum to cause regression of established tumors will be employed to determine the identity and antitumor activity of host cells which accumulate in the tumor bed to cause regression. The conversion from tumor growth to regression will be studied in relation to changes in systemic immunity and in the production of immunological effector cells in the draining lymph node. Particular attention will be given to the possibility that macrophages play an important role in this model of tumor regression.